“…The inflammation-induced increase in LN LEC proliferation coincides with type 1 interferon-induced PD-L1 overexpression on human and mouse LECs [76], although the mechanistic relevance of this association remains to be studied. Of note, other disease processes such as age-dependent accumulation of adipocytes in human LNs might cause marked loss of medullary sinus LECs and their replacement by collecting lymphatic vessels [77]; indeed, the functional consequences of such events and their disease-specific contexts remain currently unknown.…”